Double and single-stranded breaks occur in chromosomal DNA during normal cell cycle progression, or after exposure to ionizing regulation or other mutagens, or during homologous recombination. Eukaryotic cells have multiple pathways for repairing DNA breaks, as chromosomal breaks can be lethal to the cell if they are not repaired. Ends can be repaired by homologous recombination, or by joining of non-homologous ends (see, e.g., Roth et al., Mol. Cell. Biol. 5:2599-2607 (1985); Roth & Wilson, Proc. Nat'l Acad. Sci. USA 82:3355-3359 (1985)). Enzymes involved in such pathways have been implicated in diseases related to cellular proliferation, such as cancer. Thus, there is a need to establish screening assays for understanding human diseases caused by disruption of DNA repair pathways. Identifying proteins, their ligands and substrates, and downstream signal transduction pathways involved in neoplasia in humans is important for developing therapeutic regents to treat cancer and other proliferative diseases.